Cytomegalovirus (CMV) is a herpes viral genus of the Herpesviruses group thought to infect between 50% and 80% of adults in the United States. Herpesviruses share a characteristic ability to remain dormant within the body over long periods. CMV infections typically become more aggressive in patients with a depressed immune system. Patients who receive allogeneic bone marrow transplantation (aBMT) often suffer from a CMV infection due to the immunocompromising effects of treatment. Thus, there is a need to identify methods that manage CMV infections.
Vasoactive intestinal peptide (VIP) is an endogenous polypeptide that modulates both innate and adaptive immunities. The administration of VIP delays the onset, decreases the frequency, and reduces the severity of disease in various experimental models of autoimmune disease such as sepsis, collagen-induced arthritis, Crohn's disease, type-I diabetes, multiple sclerosis, pancreatitis, keratitis, and uveoretinitis. See Gonzalez-Rey, TRENDS in Molecular Medicine (2007) 13(6):241-251. It has been reported that VIP interacts with the external envelope glycoprotein (gp120) of the human immunodeficiency virus (HIV). See Redwine et al., Clin Immunol (1999) 93(2):124-31 and Peruzzi et al., AIDS Res Hum Retroviruses (2000) 16(11):1067-73. VIP is also thought to activate human CMV major immediate-early (MIE) gene expression initiating viral reactivation during latency. See Yuan et al., J Virology (2009) 83(13): 6391-6403.
Emilie et al., J Neuroimmunol., 2011, provide that vasoactive intestinal peptide receptor 1 is downregulated during expansion of antigen-specific CD8 T cells following primary and secondary Listeria monocytogenes infections. References cited herein are not an admission of prior art.